ArticleThe Journal of biological chemistry2016
Adverse Outcomes Associated with Cigarette Smoke Radicals Related to Damage to Protein-disulfide Isomerase.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- A mechanism for the disrupted redox regulation of vascular contractility during aging.iScience · 2026Article
- Endoplasmic Reticulum Stress and Unfolded Protein Response Sensor ERN1 Regulates Organic Dust Induction of Lung Inflammation.FASEB bioAdvances · 2025Article
- Effect of cigarette smoke exposure and cessation on regional diffusion properties in rat intervertebral discs.JOR spine · 2024Article
- The Multifaceted Role of Glutathione S-Transferases in Health and Disease.Biomolecules · 2023Review
- Protein disulfide isomerase A1 as a novel redox sensor in VEGFR2 signaling and angiogenesis.Angiogenesis · 2023Article
- Endoplasmic Reticulum Stress in Chronic Obstructive Pulmonary Disease: Mechanisms and Future Perspectives.Biomolecules · 2022Review
- A Synthetic Small RNA Homologous to the D-Loop Transcript of mtDNA Enhances Mitochondrial Bioenergetics.Frontiers in physiology · 2022Article
- Role of unfolded proteins in lung disease.Thorax · 2021Review
- The Impact of Endoplasmic Reticulum-Associated Protein Modifications, Folding and Degradation on Lung Structure and Function.Frontiers in physiology · 2021Review
- Ischemic stroke disrupts the endothelial glycocalyx through activation of proHPSE via acrolein exposure.The Journal of biological chemistry · 2020Article
- Retrograde signaling by a mtDNA-encoded non-coding RNA preserves mitochondrial bioenergetics.Communications biology · 2020Article
- Protein thiol oxidation in the rat lung following e-cigarette exposure.Redox biology · 2020Article
- The integrated stress response in pulmonary disease.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Endoplasmic reticulum stress and glutathione therapeutics in chronic lung diseases.Redox biology · 2020Review
- Role of the ERO1-PDI interaction in oxidative protein folding and disease.Pharmacology & therapeutics · 2020Review
- Cellular stress responses and dysfunctional Mitochondrial-cellular senescence, and therapeutics in chronic respiratory diseases.Redox biology · 2020Review
- Multi-omics systems toxicology study of mouse lung assessing the effects of aerosols from two heat-not-burn tobacco products and cigarette smoke.Computational and structural biotechnology journal · 2020Article
- Combined expression of protein disulfide isomerase and endoplasmic reticulum oxidoreductin 1-α is a poor prognostic marker for non-small cell lung cancer.Oncology letters · 2018Article
- Redox Regulation of Mitochondrial Fission Protein Drp1 by Protein Disulfide Isomerase Limits Endothelial Senescence.Cell reports · 2018Article
- Cigarette smoke modifies and inactivates SPLUNC1, leading to airway dehydration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Identification of factors contributing to the development of chronic obstructive pulmonary disease (COPD) is crucial for developing new treatments. An increase in the levels of protein-disulfide isomerase (PDI), a multifaceted endoplasmic reticulum resident chaperone, has been demonstrated in human smokers, presumably as a protective adaptation to cigarette smoke (CS) exposure. We found a similar increase in the levels of PDI in the murine model of COPD. We also found abnormally high levels (4-6 times) of oxidized and sulfenilated forms of PDI in the lungs of murine smokers compared with non-smokers. PDI oxidation progressively increases with age. We begin to delineate the possible role of an increased ratio of oxidized PDI in the age-related onset of COPD by investigating the impact of exposure to CS radicals, such as acrolein (AC), hydroxyquinones (HQ), peroxynitrites (PN), and hydrogen peroxide, on their ability to induce unfolded protein response (UPR) and their effects on the structure and function of PDIs. Exposure to AC, HQ, PN, and CS resulted in cysteine and tyrosine nitrosylation leading to an altered three-dimensional structure of the PDI due to a decrease in helical content and formation of a more random coil structure, resulting in protein unfolding, inhibition of PDI reductase and isomerase activity in vitro and in vivo, and subsequent induction of endoplasmic reticulum stress response. Addition of glutathione prevented the induction of UPR, and AC and HQ induced structural changes in PDI. Exposure to PN and glutathione resulted in conjugation of PDI possibly at active site tyrosine residues. The findings presented here propose a new role of PDI in the pathogenesis of COPD and its age-dependent onset.
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Registered trials
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